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Incidence and mortality of gynaecological cancers: Secular trends in urban Shanghai, China over 40 years.妇科癌症的发病率和死亡率：中国上海市区40年的长期趋势
Eur J Cancer. 2016 Aug;63:1-10. doi: 10.1016/j.ejca.2016.04.016. Epub 2016 May 26.
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MicroRNA-361-5p Inhibits Cancer Cell Growth by Targeting CXCR6 in Hepatocellular Carcinoma.微小RNA-361-5p通过靶向肝细胞癌中的CXCR6抑制癌细胞生长。
Cell Physiol Biochem. 2016;38(2):777-85. doi: 10.1159/000443033. Epub 2016 Feb 15.
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c-Met and CREB1 are involved in miR-433-mediated inhibition of the epithelial-mesenchymal transition in bladder cancer by regulating Akt/GSK-3β/Snail signaling.c-Met和CREB1通过调节Akt/GSK-3β/Snail信号通路参与miR-433介导的膀胱癌上皮-间质转化抑制作用。
Cell Death Dis. 2016 Feb 4;7(2):e2088. doi: 10.1038/cddis.2015.274.
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Cancer statistics in China, 2015.《中国癌症统计数据 2015》
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Ribosomal L22-like1 (RPL22L1) Promotes Ovarian Cancer Metastasis by Inducing Epithelial-to-Mesenchymal Transition.核糖体L22样蛋白1（RPL22L1）通过诱导上皮-间质转化促进卵巢癌转移。
PLoS One. 2015 Nov 30;10(11):e0143659. doi: 10.1371/journal.pone.0143659. eCollection 2015.
6
MiR-361-5p inhibits colorectal and gastric cancer growth and metastasis by targeting staphylococcal nuclease domain containing-1.微小RNA-361-5p通过靶向含葡萄球菌核酸酶结构域-1抑制结直肠癌和胃癌的生长与转移。
Oncotarget. 2015 Jul 10;6(19):17404-16. doi: 10.18632/oncotarget.3744.
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PPARγ inhibits ovarian cancer cells proliferation through upregulation of miR-125b.过氧化物酶体增殖物激活受体γ通过上调miR-125b抑制卵巢癌细胞增殖。
Biochem Biophys Res Commun. 2015 Jun 26;462(2):85-90. doi: 10.1016/j.bbrc.2015.04.023. Epub 2015 May 2.
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miR-186 regulation of Twist1 and ovarian cancer sensitivity to cisplatin.miR-186 对 Twist1 的调控及卵巢癌细胞对顺铂的敏感性
Oncogene. 2016 Jan 21;35(3):323-32. doi: 10.1038/onc.2015.84. Epub 2015 Apr 13.
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Roles of c-Met and RON kinases in tumor progression and their potential as therapeutic targets.c-Met和RON激酶在肿瘤进展中的作用及其作为治疗靶点的潜力。
Oncotarget. 2015 Feb 28;6(6):3507-18. doi: 10.18632/oncotarget.3420.
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Maintenance chemotherapy in the management of epithelial ovarian cancer.上皮性卵巢癌管理中的维持化疗
Cancer Metastasis Rev. 2015 Mar;34(1):11-7. doi: 10.1007/s10555-014-9537-x.

微小RNA-361-5p通过靶向核糖体蛋白L22样蛋白1（RPL22L1）和c-Met信号通路降低上皮性卵巢癌细胞的致瘤性。

MiR-361-5p decreases the tumorigenicity of epithelial ovarian cancer cells by targeting at RPL22L1 and c-Met signaling.

作者信息

Ma Jing, Jing Xiaotao, Chen Zhuo, Duan Zhenling, Zhang Yan

机构信息

Department of Obstetrics and Gynecology, The First Affiliated Hospital of Kunming Medical University Kunming, Yunnan, China.

出版信息

Int J Clin Exp Pathol. 2018 May 1;11(5):2588-2596. eCollection 2018.

PMID:31938372
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6958233/
Abstract

A large number of studies have shown that miRNAs are important regulators of epithelial-to-mesenchymal transition (EMT) and are associated with metastasis in epithelial ovarian cancer (EOC). MiR-361-5p has been shown to play pivotal roles in tumorigenesis and metastasis; however, a role for miR-361-5p in EOC has not been reported. In this study, we found that miR-361-5p was significantly down-regulated in EOC tissues and cell lines. In addition, over-expression of miR-361-5p inhibited the migration and invasion of EOC cells in vitro. MiR-361-5p influenced the expression of the EMT-associated proteins by upregulating the epithelial marker E-cadherin and downregulating the mesenchymal markers, N-cadherin and vimentin. Further studies identify miR-361-5p directly targeted Ribosomal L22-like1 (RPL22L1) and c-Met. Moreover, miR-361-5p repressed the Akt/mTOR pathway after c-Met inhibition. Reintroduction of RPL22L1 and c-Met reversed miR-361-5p-induced EMT suppression. Consistently, inverse correlations were also observed between the expression of miR-361-5p and RPL22L1 or c-Met in human EOC tissue samples. Taken together, miR-361-5p inhibited the EMT progression in EOC cells by targeting RPL22L1 and c-Met/Akt/mTOR signaling.

摘要

大量研究表明，微小RNA（miRNAs）是上皮-间质转化（EMT）的重要调节因子，与上皮性卵巢癌（EOC）的转移相关。已证明miR-361-5p在肿瘤发生和转移中起关键作用；然而，miR-361-5p在EOC中的作用尚未见报道。在本研究中，我们发现miR-361-5p在EOC组织和细胞系中显著下调。此外，miR-361-5p的过表达在体外抑制了EOC细胞的迁移和侵袭。miR-361-5p通过上调上皮标志物E-钙黏蛋白并下调间质标志物N-钙黏蛋白和波形蛋白来影响EMT相关蛋白的表达。进一步研究确定miR-361-5p直接靶向核糖体L22样1（RPL22L1）和c-Met。此外，c-Met抑制后，miR-361-5p抑制了Akt/mTOR通路。重新引入RPL22L1和c-Met可逆转miR-361-5p诱导的EMT抑制。同样，在人EOC组织样本中也观察到miR-361-5p与RPL22L1或c-Met表达之间呈负相关。综上所述，miR-361-5p通过靶向RPL22L1和c-Met/Akt/mTOR信号传导抑制EOC细胞中的EMT进程。